Aging and adipose tissue

This chapter describes how aging is associated with fat tissue redistribution from subcutaneous to visceral depots. This redistribution is correlated with and may cause insulin resistance and metabolic complications, as well as functional decline and mortality in the elderly. As subcutaneous fat loses its ability to store lipids, circulating fatty acids are elevated, with fatty acids being deposited ectopically, further contributing to metabolic dysfunction. Circulating free fatty acids (FFAs) are toxic to most cell types, including aged preadipocytes, potentially exacerbating fat tissue dysfunction and establishing a vicious cycle. Thus, when the main function of fat tissue, lipid storage, which requires fat cells to be able to increase in size and preadipocytes to differentiate into new fat cells, becomes dysregulated, the other functions of adipose tissue are disrupted, including immune, hormonal/paracrine regulation, and mechanical protection. Aging and obesity exert similar effects on metabolic function and share clinical consequences. Aging and obesity are both associated with increased inflammatory cytokines in adipose tissue and systemically. These cytokines, together with reduced anti-inflammatory factor generation (e.g., adiponectin, IL-10), may have a causal role in the generation of insulin resistance, impaired glucose metabolism, and systemic inflammation and are potential targets for future therapeutic interventions. However, there are notable differences between the cellular and the molecular mechanisms of fat tissue dysfunction in aging and obesity, including differences in extent of macrophage infiltration, fat cell size, and gene expression profiles.